Definition: Parkinson’s disease is a common neurological condition afflicting about 1 percent of men and women over the age of seventy. A small region in the brain, called the substantia nigra, begins to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine. With the loss of dopamine, tremors begin and movement slows. Despite current drug therapies, it remains a progressive and incurable condition. Many patients with this neurological condition may also suffer from age related cognitive decline or have some of the symptoms of Alzheimer’s disease. Parkinson’s disease is both hereditary and due to environmental factors.
Natural treatment strategies and remedies
The nutritional treatment for Parkinson’s disease is still an uncharted territory. The most promising approach appears to be the use of antioxidants to slow the oxidation and damage to the substantia nigra. It’s possible that additional nutritional approaches may be found in the future. Those who exercise regularly early in their adult life have a lower risk. Weight training in a gym or at home could reduce the stiffness, slowness, and tremors.
Over the past few decades, doctors have made important advances in the treatment of Parkinson’s disease with pharmaceutical medicines. Yet, several nutritional treatment strategies exist which should be explored further.
Improving the antioxidant system
Of all the nutritional treatments available for Parkinson’s disease, antioxidants appear to be the most promising choices to prevent or slow the progression of this condition. Individuals whose diets include plenty of healthy foods containing antioxidants are less likely to develop this neurological condition. Patients should consume foods, such as fruits and vegetables that containglutathione or can help produce it. Cyanohydroxybutene, a chemical found in broccoli, cauliflower, Brussels sprouts and cabbage, is also thought to increase glutathione levels. Anthocyanins are antioxidants found in berries that could be of benefit. High intake of dairy products may lead to a higher incidence of Parkinson’s disease.
The following antioxidants may be helpful in addition to standard pharmaceutical therapy. Please use low dosages initially until you learn how each supplement works for you before upping the dose. Also, combining supplements and medicines can sometimes have a stimulating effect. Learn how each supplement works by itself before adding another one.
Mucuna pruriens is an herb to seriously consider for Parkinson’s disease. It has been successfully used in India for centuries. Mucuna may work as an antioxidant and also as a dopamine provider. We know little about the ideal dosage of mucuna to treat Parkinson’s disease.
R-alpha lipoic acid 10 to 50 mg a few times a week in the morning with breakfast. R-Lipoic acid is a powerful antioxidant and helps generate glutathione. Alpha lipoic acid may be used in combination with Acetyl-l-Carnitine as a treatment for Parkinson’s disease. The proper dosage of the combination of alpha lipoic acid and acety l carnitine as a treatment for Parkinson’s disease remains to be determined, but it may be a good idea to start at a low dosage of 30 mg of R ALA and less than 300 mg of acetyl l carnitine for a few days before considering taking higher amounts. The interaction of these supplements with medications currently used for Parkinson’s disease is not clear, nor is their interaction with mucuna pruriens and other natural herbs and supplements.
Combined R-alpha-lipoic acid and acetyl-L-carnitine exerts efficient preventative effects in a cellular model of Parkinson’s disease.
J Cell Mol Med. 2008.
Mitochondrial dysfunction and oxidative damage are highly involved in the pathogenesis of Parkinson’s disease. Some mitochondrial antioxidants / nutrients that can improve mitochondrial function and/or attenuate oxidative damage have been implicated in Parkinson’s disease therapy. The present study examined the preventative effects of two mitochondrial antioxidant / nutrients, R-alpha-lipoic acid and acetyl-L-carnitine. We demonstrated that 4-week pretreatment with R-alpha-lipoic acid and/or acetyl-L-carnitine effectively protected SK-N-MC human neuroblastoma cells against rotenone-induced mitochondrial dysfunction, oxidative damage, and accumulation of alpha-synuclein and ubiquitin. Most notably, we found that when combined, R-alpha-lipoic acid and acetyl-L-carnitine worked at 100 to 1000 fold lower concentrations than they did individually.
CoQ10 — this nutrient helps preserve dopaminergic neurons from toxins. A dose of 20 mg to 50 mg a few mornings a week with breakfast is reasonable. This nutrient also improves energy production in cells. However, research with CoQ10 and Parkinson’s disease has provided mixed findings, and there is not convincing evidence that the use of CoQ10 will have a significant effect on the symptoms of Parkinson’s disease. CoQ10, though, is a healthy supplement, and low doses could be beneficial for other purposes besides Parkinson’s disease.
Natural vitamin E complex between 30 and 200 units a few times a week preferably of mixed, natural tocopherols taken with any meal. Eating food rich in vitamin E may help protect against Parkinson’s disease. Foods rich in the vitamin include nuts, seeds, wheat germ, spinach and other green leafy vegetables.
Natural vitamin C with bioflavonoids between 100 and 300 mg once or twice a day. In addition to being an antioxidant, vitamin C also helps the production of L-dopa from tyrosine.
N-acetyl-cysteine is an antioxidant that can help regenerate glutathione. A dose of 100 to 250 mg of NAC can be taken most mornings before breakfast.
Quercetin, a flavonoid, may be of benefit.
Selenium is an antioxidant that can help increase levels of glutathione. A dose of 50 to 100 micrograms a day can be taken with any meal. Selenium is also normally found in multivitamin and mineral pills.
Melatonin is the sleep hormone with antioxidant abilities. A dose of 0.3 to 1 mg can be taken one or three hours before bed for those with insomnia. Tolerance can develop with regular use and since we don’t know the long-term effects of nightly use, it’s best to limit the frequency of use of melatonin to once or twice a week. In the 1980s, some individuals taking a synthetic drug called MPTP developed symptoms similar to Parkinson’s disease. It was determined that MPTP causes an oxidative destruction of substantia nigra neurons. Interestingly, a study with rats has determined that the administration of melatonin is able to almost completely prevent the neurotoxicity from MPP, a toxin very similar to MPTP. The rats on melatonin and MPP did not get symptoms of Parkinson’s disease while the controls on MPP alone did.
Withania somnifera, also known as ashwagandha, was found in a rodent study to be helpful for tardive dyskinesia symptoms although it is not known whether ashwagandha would be helpful in dyskinesia due to L-DOPA induce dyskinesia.
Providing dopamine precursors
L-dopa, the immediate precursor to dopamine, is a nutrient available by prescription. L-dopa (often combined with carbidopa) is the most commonly used medicine to treat Parkinson’s disease. It is possible that the use of L-dopa for prolonged periods causes oxidation and toxicity to brain cells. If this turns out to be true, it would further justify the recommendations that antioxidants be added to standard Parkinson’s disease therapy. There is, as of yet, no clinical proof that taking antioxidant supplements help those with Parkinson’s disease live longer but all indications point to the possibility that the course of the disease can be slowed by providing adequate antioxidant support.
Tyrosine is an amino acid that can be converted into L-dopa. But there is no reason to take tyrosine if L-dopa is available. Another way to increase dopamine levels is with the use of B vitamins, particularly NADH. Preliminary studies have shown some benefit with NADH in the therapy of PD. Although more research is needed, for the time being, it would seem reasonable to add NADH at a dose of 2.5 mg. NADH can be taken every other morning on an empty stomach. NADH may also help regenerate the antioxidant glutathione which could be beneficial. Be careful when you add NADH when you are already taking L-dopa or other medicines that treat Parkinson’s disease, since the effects could be cumulative. The long-term effectiveness of NADH in patients with Parkinson’s disease is currently not known. Taking between one to three times the RDA for the B vitamins seems to be a reasonable option.
Blocking dopamine breakdown
Dopamine is broken down in the brain by an enzyme called monoamine oxidase (MAO). When the activity of MAO is inhibited, dopamine stays around longer and this benefits those with Parkinson’s disease. Several drugs are available that block the activity of MAO. Selegiline is the most effective and the one used most commonly. The prescribed dosage is 5 mg a day.
No nutrients are currently known that prevent the breakdown of dopamine. However, a study conducted on rats at the College of Humanities and Sciences, Beijing Union University, in Beijing, China, indicates that the Chinese herbs codonopsis and astragalus can inhibit MAO type B and increase the activity of the antioxidant SOD. We don’t have any human trials to determine whether these two herbs would benefit patients with Parkinson’s disease. Although selegiline is a very helpful medicine, high doses may increase the risk of heart irregularities.
Additional nutrients and supplements to consider
Some of the following nutrients may not be directly involved in making more dopamine, but could well improve general cognitive abilities or provide other benefits. Many patients who have Parkinson’s disease, especially the elderly, have age related cognitive decline. You may also consider drinking less milk (see below).
Fish oils at 500 to 1,000 mg a day of EPA / DHA with meals. The role of fish oils in Parkinson’s disease is being evaluated since omega-3 fatty acids can generally improve overall brain health. Each fish oil softgel usually has about 300 mg of a combination epa and dha fatty acids.
Depression in Parkinson’s disease: a double-blind, randomized, placebo-controlled pilot study of omega-3 fatty-acid supplementation.
J Affect Disord. 2008. Laboratório de Neurofisiologia, Departamento de Fisiologia, Universidade Federal do Paraná, C.P, Curitiba, PR, Brazil.
Our results reveal that PD patients taking fish oil, with or without antidepressants, presented improvement in depressive symptoms and indicate that the intake of omega-3 can be used with an antidepressant effect or as adjuvant therapy with some other medication. This is a first pilot study with parkinsonian patients and omega-3 supplementation and requires replication in a larger sample.
Gingko biloba at 40 mg most days with breakfast or lunch. This herb has antioxidant properties and helps improve memory and alertness.
Neuroprotective effect of Ginkgo biloba L. extract in a rat model of Parkinson disease.
Phytother Res. 2004.
Our data suggest that the neuroprotective effects of Ginkgo biloba reduce the behavioural deficit in 6-hydroxydopamine lesions in rat and also indicates a possible role for the extract in the treatment of Parkinson’s disease.
Replacing hormones in patients with Parkinson’s disease may be an additional option. Whether pregnenolone, DHEA, or other hormones are helpful in Parkinson’s disease is currently not known. Long term use of high doses of hormones has side effects.
Calcium and vitamin D supplements may be helpful for bone health. People with Parkinson’s disease have an elevated risk of developing fragile bones and fractures. Reduced mobility can lead to reduced bone mass and a greater risk of falls — which together put Parkinson’s disease patients at risk of bone fractures and joint injuries.
It’s quite likely that the proper use of natural supplements can reduce the necessary dose of L-dopa, selegiline, and other drugs currently used to treat Parkinson’s disease, or help slow down the progression of the condition. There’s still a great deal we need to learn about the nutritional treatment of PD.
Treadmill training can help Parkinson’s patients to walk more normally. However, it’s unclear how long the benefits of treadmill training will last, or the best way to deliver this type of training to patients with the movement disorder. The Cochrane Library 2010.
Although Parkinson’s disease can occur from viral infections or exposure to environmental toxins, such as pesticides, the causes of the majority of cases are not well known. Scientists suspect that oxidative damage to neurons in the substantia nigra could well be one of the major causes, particularly due to the depletion of the antioxidant glutathione. There can be an overlap betweendementia and PD.
People living near a steel factory or another source of high manganese emissions are at higher risk.
Researchers at the University of Aberdeen in Scotland have discovered that the more pesticides gardeners are exposed to, the more likely they are to develop the degenerative brain disease. The results reinforce the need for amateur gardeners and farmers alike to wear protective equipment when spraying pesticides. Amateur gardeners were 9 percent more likely to suffer from the disease than non-pesticide users. Farmers were 43 percent more likely.
Consumption of milk and calcium in midlife and the future risk of Parkinson disease
Middle-aged men who drink a glass or two of milk each day may be increasing their risk later in life. The ingredient or possible contaminant in milk responsible for this effect is unclear, but the current findings suggest it’s not the calcium.
Parkinson’s disease fact : the four most popular Parkinsonian neurotoxins are 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat.
People who sustain substantial head injuries face an increased risk of developing Parkinson’s disease years later. This has been shown in more than one study, therefore, it is safe to assume that head injury, such as in boxing, is a cause.
Taking prescription amphetamines may raise your risk years later.
Individuals with Parkinson’s disease have tremor of the hands, rigidity, poor balance, and mild intellectual deterioration. The tremor is most apparent at rest and is less severe with movement.Shaking or tremor is an early symptom of Parkinson’s disease. Progression leads to trembling in arms, legs, jaw, and rigidity or stiffness of the limbs.
It is difficult to diagnose Parkinson’s disease in the early stages. Early on, PD is diagnosed almost primarily by its symptoms, and studies indicate that physicians make an incorrect initial diagnosis of Parkinson’s disease in between 10% and 40% of cases. Blood tests are not helpful for diagnosis.
Common medicines used in Parkinson’s disease to improve prognosis
There are basically three types of Parkinson’s disease drugs that are commonly prescribed for patients with Parkinson’s disease. First, doctors prescribe dopamine precursor medication, such as L-dopa, which converts into dopamine. A second medication type is using drugs that block the breakdown of dopamine. A common medicine used for this purpose is selegiline (also known as deprenyl). And third, drugs are provided that influence dopamine receptors directly. The two most commonly prescribed are bromocriptine and pergolide. Researchers from the Mayo Clinic say that in some cases, patients taking pergolide (Permax) may experience damage to heart valves. In some cases, patients taking cabergoline may experience damage to heart valves. High cumulative doses of and long-term treatment with cabergoline ( Dostinex ) are risk factors for the development of valvulopathy.
Some develope a gambling problem while taking Mirapex or similar drugs.
Dopamine agonists may trigger sudden uncontrollable sleepiness in about one in five patients. About one in five patients taking a therapeutic dose of a dopamine agonist develop compulsive gambling or hypersexuality.
Although symptoms of Parkinson’s disease often improve when the drug levodopa is given, brain scan results suggest that the drug hastens progression of the disease, according to a report in The New England Journal of Medicine. Given these conflicting findings, the long-term effects of levodopa on the disease remain unclear. The researchers evaluated 361 patients with early Parkinson’s disease who were treated with levodopa at one of three doses or with inactive placebo for 40 weeks. The main outcome measure was the extent to which symptoms worsened during treatment, but a subgroup of patients was also evaluated with brain scans. Parkinson’s symptoms worsened to a lesser extent in patients who received levodopa, at any dose, than in those who received placebo. In contrast, brain scanning in 116 patients showed that patients treated with levodopa lost more critical nerve cells than those who received placebo.
Dr. Sahelian comments: perhaps levodopa acts as an oxidant, damaging nerve cells.
I was diagnosed with PD in 2005. At that time I was prescribed with Artane (Benzhexol hydrochloride 2 mg) and still taking this medicine until today. In 2009 I started taking Mucuna Pruriens and over last 6 months I took 2 times/day with 40 % L-Dopa. In July 2009 I suffered from eyelids disorder (involuntary spasm of the eyelids muscle) and today the condition is getting bad. With PD getting bad over the past 2 years, I felt de-motivated, stressed and find myself useless due these sickness. I went to see eye specialists in 2010 and confirmed the eyes are good.
New Parkinson’s Drug
In 2006 FDA approved Azilect (rasagiline) for the treatment of Parkinson’s disease. Axilect is a monoamine oxidase type–B (MAO-B) inhibitor that blocks the breakdown of dopamine, a chemical that sends information to the parts of the brain that control movement and coordination. Azilect was approved for use as an initial single drug therapy in early Parkinson’s disease, and as an addition to levodopa in more advanced patients. Levodopa is a standard treatment for Parkinson’s disease.